When breathing normally, one's diaphragm is dropped to increase one's thoracic cavity, thus creating a negative pressure in the thoracic cavity, relative to atmospheric pressure. Air is driven by the atmospheric pressure into the negative-pressure thoracic cavity. Many patients, such as victims of accidents suffering from shock, trauma or heart attack, may require a respirator or ventilator to aid breathing. Prior respirators used intermittent, positive pressure breaths to increase the pressure within a patient's lungs until filled. Air is expelled passively by the natural stiffness of the lungs.
Such respirators drive a positive pressure breath into the lungs which are already at atmospheric pressure. The pressure in the lungs is increased above atmospheric pressure, contrary to normal occurrence, which inhibits the heart's ability to pump blood. During normal respiration, negative thoracic pressure is developed upon inspiration of air, which aids in filling the heart with blood. The resultant pressure gradient (the relatively positive pressure in the periphery and negative pressure in the thorax) helps to fill the heart as it opens, subsequent to the heart's squeezing or pumping motion. If however, the pressure in the thoracic chamber is increased, as with respirators, the amount of blood returning or entering the heart is decreased. The heart also must squeeze against a higher pressure. A lower cardiac output results.
The common technique for improving arterial oxygen tension is the use of Positive-End-Expiratory Pressure (PEEP), where a low level of positive pressure is maintained in the airway between positive pressure breaths. PEEP uses a standard switch. A pressure signal applied to the valve controls the high or low pressure states of the valve. The low PEEP state is generated when the valve is fully open. A partial closing of the valve creates high intrathoracic pressure between breaths, as some air from the tidal volume is not allowed to escape. However, at 10 centimeters of water pressure of PEEP, cardiac output drops significantly. Intravenous fluids are used to increase intravascular volume in an effort to minimize this fall in cardiac output. The patient may already have compromised cardiac function, minimizing or negating the advantages of the intravascular volume increase. Additionally, patients requiring respirators typically lack adequate kidney function and cannot process the added fluids. If too much intravenous fluid is used, relative to the patient's ability (aided or not) to process the fluid, the fluid may enter the patient's lungs.
Positive inotropic agents are used to increase the squeeze of the heart to pump more blood. Obviously, the heart works harder than normal resulting in possible heart attacks or arrhythmias. Often, physicians will prescribe a combination of increased intravenous fluids and positive inotropic agents with PEEP.
Several investigators have evaluated the effect of cardiac cycle-specified, increases in thoracic pressure on cardiac output. They synchronized high frequency jet ventilation to various phases of the R-R interval. Carlson and Pinsky found that the cardiac depressant effect of positive pressure ventilation is minimized if the positive pressure pulsations are synchronized with diasrole. Otto and Tyson, however, found no significant changes in cardiac output while synchronizing positive pressure pulsations to various portions of the cardiac cycle.
Pinchak described the best frequency in high frequency jet ventilation. He also noticed rhythmic oscillations in pulmonary artery pressure (PAP) and also rhythmic changes in systemic blood pressure. A possible explanation for these oscillations is that the jet pulsations move in and out of synchrony with the heart rate. In evaluating his data it appears that when jet airway pressure peak occurred during early systole there was a high pulmonary artery pressure, and a low systemic blood pressure. While Pinchak does not comment on this, his recorded data show that pulmonary artery pressure was waxing and waning precisely opposite to the blood pressure. A plausible explanation is an increase in pulmonary artery pressure is simply a reflection of an increase in pulmonary vascular resistance which causes a decrement in left ventricular filling and thus decrease in systemic blood pressure secondary to a decrease in cardiac output. If the slight oscillations in the systemic blood pressure reflect oscillations in cardiac output, then Pinchak's study would support Pinsky and Carlson's work, suggesting that positive airway pressure is least detrimental during diastole.